The Experts below are selected from a list of 57 Experts worldwide ranked by ideXlab platform
Jan Jensen - One of the best experts on this subject based on the ideXlab platform.
-
Growth Factor Independence-1 (Gfi1) Is Required for Pancreatic Acinar Unit Formation and Centroacinar Cell DifferentiationSummary
Elsevier, 2015Co-Authors: Pia Nyeng, Fan Xiao, Jorge Dorantes, Jan JensenAbstract:Background & Aims: The genetic specification of the compartmentalized pancreatic acinar/Centroacinar unit is poorly understood. Growth factor independence-1 (Gfi1) is a zinc finger transcriptional repressor that regulates hematopoietic stem Cell maintenance, pre-T-Cell differentiation, formation of granulocytes, inner ear hair Cells, and the development of secretory Cell types in the intestine. As GFI1/Gfi1 is expressed in human and rodent pancreas, we characterized the potential function of Gfi1 in mouse pancreatic development. Methods: Gfi1 knockout mice were analyzed at histological and molecular levels, including qRT-PCR, in situ hybridization, immunohistochemistry, and electron microscopy. Results: Loss of Gfi1 impacted formation and structure of the pancreatic acinar/Centroacinar unit. Histologic and ultrastructural analysis of Gfi1-null pancreas revealed specific defects at the level of pancreatic acinar Cells as well as the Centroacinar Cells (CACs) in Gfi1â/â mice when compared with wild-type littermates. Pancreatic endocrine differentiation, islet architecture, and function were unaffected. Organ domain patterning and the formation of ductal Cells occurred normally during the murine secondary transition (E13.5âE14.5) in the Gfi1â/â pancreas. However, at later gestational time points (E18.5), expression of Cellular markers for CACs was substantially reduced in Gfi1â/â mice, corroborated by electron microscopy imaging of the acinar/Centroacinar unit. The reduction in CACs was correlated with an exocrine organ defect. Postnatally, Gfi1 deficiency resulted in severe pancreatic acinar dysplasia, including loss of granulation, autolytic vacuolation, and a proliferative and apoptotic response. Conclusions: Gfi1 plays an important role in regulating the development of pancreatic CACs and the function of pancreatic acinar Cells. Keywords: Centroacinar Cells, Claudin 10, Growth Factor Independence-1 (Gfi1
-
Growth Factor Independence-1 (Gfi1) Is Required for Pancreatic Acinar Unit Formation and Centroacinar Cell Differentiation
Cellular and molecular gastroenterology and hepatology, 2014Co-Authors: Pia Nyeng, Fan Xiao, Jorge Dorantes, Jan JensenAbstract:Background & Aims The genetic specification of the compartmentalized pancreatic acinar/Centroacinar unit is poorly understood. Growth factor independence-1 (Gfi1) is a zinc finger transcriptional repressor that regulates hematopoietic stem Cell maintenance, pre-T-Cell differentiation, formation of granulocytes, inner ear hair Cells, and the development of secretory Cell types in the intestine. As GFI1/Gfi1 is expressed in human and rodent pancreas, we characterized the potential function of Gfi1 in mouse pancreatic development. Methods Gfi1 knockout mice were analyzed at histological and molecular levels, including qRT-PCR, in situ hybridization, immunohistochemistry, and electron microscopy. Results Loss of Gfi1 impacted formation and structure of the pancreatic acinar/Centroacinar unit. Histologic and ultrastructural analysis of Gfi1-null pancreas revealed specific defects at the level of pancreatic acinar Cells as well as the Centroacinar Cells (CACs) in Gfi1−/− mice when compared with wild-type littermates. Pancreatic endocrine differentiation, islet architecture, and function were unaffected. Organ domain patterning and the formation of ductal Cells occurred normally during the murine secondary transition (E13.5–E14.5) in the Gfi1−/− pancreas. However, at later gestational time points (E18.5), expression of Cellular markers for CACs was substantially reduced in Gfi1−/− mice, corroborated by electron microscopy imaging of the acinar/Centroacinar unit. The reduction in CACs was correlated with an exocrine organ defect. Postnatally, Gfi1 deficiency resulted in severe pancreatic acinar dysplasia, including loss of granulation, autolytic vacuolation, and a proliferative and apoptotic response. Conclusions Gfi1 plays an important role in regulating the development of pancreatic CACs and the function of pancreatic acinar Cells.
Yoshikazu Kinoshita - One of the best experts on this subject based on the ideXlab platform.
-
Three-dimensional structure of peripheral exocrine gland in rat pancreas: reconstruction using transmission electron microscopic examination of serial sections.
Pancreas, 2005Co-Authors: Nobuo Ashizawa, Toshio Sakai, Tsunao Yoneyama, Hiroyuki Naora, Yoshikazu KinoshitaAbstract:The purpose of this study was to elucidate the 3-dimensional structure of the peripheral pancreatic exocrine gland. We observed serial sections of rat pancreatic tissue using a transmission electron microscope and traced the intercalated duct lumina, intra-acinar secretory canaliculi, intercalated duct Cells or Centroacinar Cells, and basement membranes of acini onto a transparent sheet. These traced diagrams were reconstructed. The intra-acinar secretory canaliculus had branches but no anastomosis. The interCellular secretory canaliculus was extended from the central lumen through the space between the lateral surfaces of the acinar Cells to the acinar base. Furthermore, the cytoplasmic process of each Centroacinar Cell was extended along the central lumen and connected to an intercalated duct Cell; thus, Centroacinar Cells with the same structure as intercalated duct Cells were not isolated from the intercalated duct Cells. In this study, we elucidated the normal 3-dimensional structure of the peripheral pancreatic exocrine gland. To understand the pathogenesis of chronic pancreatitis, in the future we intend to examine the morphologic changes of pancreatic tissue during the onset and advancement of chronic pancreatitis using animal models.
-
Three-dimensional structure of peripheral exocrine gland in rat pancreas: reconstruction using transmission electron microscopic examination of serial sections.
Pancreas, 2005Co-Authors: Nobuo Ashizawa, Toshio Sakai, Tsunao Yoneyama, Hiroyuki Naora, Yoshikazu KinoshitaAbstract:OBJECTIVES The purpose of this study was to elucidate the 3-dimensional structure of the peripheral pancreatic exocrine gland. METHODS We observed serial sections of rat pancreatic tissue using a transmission electron microscope and traced the intercalated duct lumina, intra-acinar secretory canaliculi, intercalated duct Cells or Centroacinar Cells, and basement membranes of acini onto a transparent sheet. These traced diagrams were reconstructed. RESULTS The intra-acinar secretory canaliculus had branches but no anastomosis. The interCellular secretory canaliculus was extended from the central lumen through the space between the lateral surfaces of the acinar Cells to the acinar base. Furthermore, the cytoplasmic process of each Centroacinar Cell was extended along the central lumen and connected to an intercalated duct Cell; thus, Centroacinar Cells with the same structure as intercalated duct Cells were not isolated from the intercalated duct Cells. CONCLUSIONS In this study, we elucidated the normal 3-dimensional structure of the peripheral pancreatic exocrine gland. To understand the pathogenesis of chronic pancreatitis, in the future we intend to examine the morphologic changes of pancreatic tissue during the onset and advancement of chronic pancreatitis using animal models.
Pia Nyeng - One of the best experts on this subject based on the ideXlab platform.
-
Growth Factor Independence-1 (Gfi1) Is Required for Pancreatic Acinar Unit Formation and Centroacinar Cell DifferentiationSummary
Elsevier, 2015Co-Authors: Pia Nyeng, Fan Xiao, Jorge Dorantes, Jan JensenAbstract:Background & Aims: The genetic specification of the compartmentalized pancreatic acinar/Centroacinar unit is poorly understood. Growth factor independence-1 (Gfi1) is a zinc finger transcriptional repressor that regulates hematopoietic stem Cell maintenance, pre-T-Cell differentiation, formation of granulocytes, inner ear hair Cells, and the development of secretory Cell types in the intestine. As GFI1/Gfi1 is expressed in human and rodent pancreas, we characterized the potential function of Gfi1 in mouse pancreatic development. Methods: Gfi1 knockout mice were analyzed at histological and molecular levels, including qRT-PCR, in situ hybridization, immunohistochemistry, and electron microscopy. Results: Loss of Gfi1 impacted formation and structure of the pancreatic acinar/Centroacinar unit. Histologic and ultrastructural analysis of Gfi1-null pancreas revealed specific defects at the level of pancreatic acinar Cells as well as the Centroacinar Cells (CACs) in Gfi1â/â mice when compared with wild-type littermates. Pancreatic endocrine differentiation, islet architecture, and function were unaffected. Organ domain patterning and the formation of ductal Cells occurred normally during the murine secondary transition (E13.5âE14.5) in the Gfi1â/â pancreas. However, at later gestational time points (E18.5), expression of Cellular markers for CACs was substantially reduced in Gfi1â/â mice, corroborated by electron microscopy imaging of the acinar/Centroacinar unit. The reduction in CACs was correlated with an exocrine organ defect. Postnatally, Gfi1 deficiency resulted in severe pancreatic acinar dysplasia, including loss of granulation, autolytic vacuolation, and a proliferative and apoptotic response. Conclusions: Gfi1 plays an important role in regulating the development of pancreatic CACs and the function of pancreatic acinar Cells. Keywords: Centroacinar Cells, Claudin 10, Growth Factor Independence-1 (Gfi1
-
Growth Factor Independence-1 (Gfi1) Is Required for Pancreatic Acinar Unit Formation and Centroacinar Cell Differentiation
Cellular and molecular gastroenterology and hepatology, 2014Co-Authors: Pia Nyeng, Fan Xiao, Jorge Dorantes, Jan JensenAbstract:Background & Aims The genetic specification of the compartmentalized pancreatic acinar/Centroacinar unit is poorly understood. Growth factor independence-1 (Gfi1) is a zinc finger transcriptional repressor that regulates hematopoietic stem Cell maintenance, pre-T-Cell differentiation, formation of granulocytes, inner ear hair Cells, and the development of secretory Cell types in the intestine. As GFI1/Gfi1 is expressed in human and rodent pancreas, we characterized the potential function of Gfi1 in mouse pancreatic development. Methods Gfi1 knockout mice were analyzed at histological and molecular levels, including qRT-PCR, in situ hybridization, immunohistochemistry, and electron microscopy. Results Loss of Gfi1 impacted formation and structure of the pancreatic acinar/Centroacinar unit. Histologic and ultrastructural analysis of Gfi1-null pancreas revealed specific defects at the level of pancreatic acinar Cells as well as the Centroacinar Cells (CACs) in Gfi1−/− mice when compared with wild-type littermates. Pancreatic endocrine differentiation, islet architecture, and function were unaffected. Organ domain patterning and the formation of ductal Cells occurred normally during the murine secondary transition (E13.5–E14.5) in the Gfi1−/− pancreas. However, at later gestational time points (E18.5), expression of Cellular markers for CACs was substantially reduced in Gfi1−/− mice, corroborated by electron microscopy imaging of the acinar/Centroacinar unit. The reduction in CACs was correlated with an exocrine organ defect. Postnatally, Gfi1 deficiency resulted in severe pancreatic acinar dysplasia, including loss of granulation, autolytic vacuolation, and a proliferative and apoptotic response. Conclusions Gfi1 plays an important role in regulating the development of pancreatic CACs and the function of pancreatic acinar Cells.
Nobuo Ashizawa - One of the best experts on this subject based on the ideXlab platform.
-
Three-dimensional structure of peripheral exocrine gland in rat pancreas: reconstruction using transmission electron microscopic examination of serial sections.
Pancreas, 2005Co-Authors: Nobuo Ashizawa, Toshio Sakai, Tsunao Yoneyama, Hiroyuki Naora, Yoshikazu KinoshitaAbstract:The purpose of this study was to elucidate the 3-dimensional structure of the peripheral pancreatic exocrine gland. We observed serial sections of rat pancreatic tissue using a transmission electron microscope and traced the intercalated duct lumina, intra-acinar secretory canaliculi, intercalated duct Cells or Centroacinar Cells, and basement membranes of acini onto a transparent sheet. These traced diagrams were reconstructed. The intra-acinar secretory canaliculus had branches but no anastomosis. The interCellular secretory canaliculus was extended from the central lumen through the space between the lateral surfaces of the acinar Cells to the acinar base. Furthermore, the cytoplasmic process of each Centroacinar Cell was extended along the central lumen and connected to an intercalated duct Cell; thus, Centroacinar Cells with the same structure as intercalated duct Cells were not isolated from the intercalated duct Cells. In this study, we elucidated the normal 3-dimensional structure of the peripheral pancreatic exocrine gland. To understand the pathogenesis of chronic pancreatitis, in the future we intend to examine the morphologic changes of pancreatic tissue during the onset and advancement of chronic pancreatitis using animal models.
-
Three-dimensional structure of peripheral exocrine gland in rat pancreas: reconstruction using transmission electron microscopic examination of serial sections.
Pancreas, 2005Co-Authors: Nobuo Ashizawa, Toshio Sakai, Tsunao Yoneyama, Hiroyuki Naora, Yoshikazu KinoshitaAbstract:OBJECTIVES The purpose of this study was to elucidate the 3-dimensional structure of the peripheral pancreatic exocrine gland. METHODS We observed serial sections of rat pancreatic tissue using a transmission electron microscope and traced the intercalated duct lumina, intra-acinar secretory canaliculi, intercalated duct Cells or Centroacinar Cells, and basement membranes of acini onto a transparent sheet. These traced diagrams were reconstructed. RESULTS The intra-acinar secretory canaliculus had branches but no anastomosis. The interCellular secretory canaliculus was extended from the central lumen through the space between the lateral surfaces of the acinar Cells to the acinar base. Furthermore, the cytoplasmic process of each Centroacinar Cell was extended along the central lumen and connected to an intercalated duct Cell; thus, Centroacinar Cells with the same structure as intercalated duct Cells were not isolated from the intercalated duct Cells. CONCLUSIONS In this study, we elucidated the normal 3-dimensional structure of the peripheral pancreatic exocrine gland. To understand the pathogenesis of chronic pancreatitis, in the future we intend to examine the morphologic changes of pancreatic tissue during the onset and advancement of chronic pancreatitis using animal models.
Fan Xiao - One of the best experts on this subject based on the ideXlab platform.
-
Growth Factor Independence-1 (Gfi1) Is Required for Pancreatic Acinar Unit Formation and Centroacinar Cell DifferentiationSummary
Elsevier, 2015Co-Authors: Pia Nyeng, Fan Xiao, Jorge Dorantes, Jan JensenAbstract:Background & Aims: The genetic specification of the compartmentalized pancreatic acinar/Centroacinar unit is poorly understood. Growth factor independence-1 (Gfi1) is a zinc finger transcriptional repressor that regulates hematopoietic stem Cell maintenance, pre-T-Cell differentiation, formation of granulocytes, inner ear hair Cells, and the development of secretory Cell types in the intestine. As GFI1/Gfi1 is expressed in human and rodent pancreas, we characterized the potential function of Gfi1 in mouse pancreatic development. Methods: Gfi1 knockout mice were analyzed at histological and molecular levels, including qRT-PCR, in situ hybridization, immunohistochemistry, and electron microscopy. Results: Loss of Gfi1 impacted formation and structure of the pancreatic acinar/Centroacinar unit. Histologic and ultrastructural analysis of Gfi1-null pancreas revealed specific defects at the level of pancreatic acinar Cells as well as the Centroacinar Cells (CACs) in Gfi1â/â mice when compared with wild-type littermates. Pancreatic endocrine differentiation, islet architecture, and function were unaffected. Organ domain patterning and the formation of ductal Cells occurred normally during the murine secondary transition (E13.5âE14.5) in the Gfi1â/â pancreas. However, at later gestational time points (E18.5), expression of Cellular markers for CACs was substantially reduced in Gfi1â/â mice, corroborated by electron microscopy imaging of the acinar/Centroacinar unit. The reduction in CACs was correlated with an exocrine organ defect. Postnatally, Gfi1 deficiency resulted in severe pancreatic acinar dysplasia, including loss of granulation, autolytic vacuolation, and a proliferative and apoptotic response. Conclusions: Gfi1 plays an important role in regulating the development of pancreatic CACs and the function of pancreatic acinar Cells. Keywords: Centroacinar Cells, Claudin 10, Growth Factor Independence-1 (Gfi1
-
Growth Factor Independence-1 (Gfi1) Is Required for Pancreatic Acinar Unit Formation and Centroacinar Cell Differentiation
Cellular and molecular gastroenterology and hepatology, 2014Co-Authors: Pia Nyeng, Fan Xiao, Jorge Dorantes, Jan JensenAbstract:Background & Aims The genetic specification of the compartmentalized pancreatic acinar/Centroacinar unit is poorly understood. Growth factor independence-1 (Gfi1) is a zinc finger transcriptional repressor that regulates hematopoietic stem Cell maintenance, pre-T-Cell differentiation, formation of granulocytes, inner ear hair Cells, and the development of secretory Cell types in the intestine. As GFI1/Gfi1 is expressed in human and rodent pancreas, we characterized the potential function of Gfi1 in mouse pancreatic development. Methods Gfi1 knockout mice were analyzed at histological and molecular levels, including qRT-PCR, in situ hybridization, immunohistochemistry, and electron microscopy. Results Loss of Gfi1 impacted formation and structure of the pancreatic acinar/Centroacinar unit. Histologic and ultrastructural analysis of Gfi1-null pancreas revealed specific defects at the level of pancreatic acinar Cells as well as the Centroacinar Cells (CACs) in Gfi1−/− mice when compared with wild-type littermates. Pancreatic endocrine differentiation, islet architecture, and function were unaffected. Organ domain patterning and the formation of ductal Cells occurred normally during the murine secondary transition (E13.5–E14.5) in the Gfi1−/− pancreas. However, at later gestational time points (E18.5), expression of Cellular markers for CACs was substantially reduced in Gfi1−/− mice, corroborated by electron microscopy imaging of the acinar/Centroacinar unit. The reduction in CACs was correlated with an exocrine organ defect. Postnatally, Gfi1 deficiency resulted in severe pancreatic acinar dysplasia, including loss of granulation, autolytic vacuolation, and a proliferative and apoptotic response. Conclusions Gfi1 plays an important role in regulating the development of pancreatic CACs and the function of pancreatic acinar Cells.